Selective transplantation of purified erythrocyte precursors will be evaluated as a method to correct defective erythrocytopoiesis. This procedure offers the potential of supplying a new population of normal erythrocytes capable of replicating and repopulating the bone marrow. As such, it suggests a therapeutic procedure which may be applicable in controlling genetically mediated erythrocyte diseases such as thalassemia. It may also be useful in reversing clinical states characterized by precursor erythrocyte depletion. The proposed approach may be employed while minimizing the risk of initiating graft vs host reactions or stimulating histocompatibility mediated rejection. Prior studies have indicated that fetal liver cells act as a predominantly erythrocyte precursor population. Pleuripotent stem cells capable of emerging as immunocompetent lymphocytes are present in the fetal liver, but in restricted numbers. Successful erythrocyte repopulation does not depend on survival or proliferation of such lymphocytes. Accordingly, the proposed study intends to selectively inhibit lymphocyte growth from fetal liver without interfering with erythrocyte reconstitution. This will be accomplished by antithymocyte antisera, oxisuran and extracts from the seeds of Ulex europeous. A model experimental animal system with a genetic defect of erythrocytes has been developed for this purpose. Colonies of non-isologous deer mice that are hematologically normal or else have hereditary spherocytosis will be employed. The study will determine the optimum gestational ages and numbers of fetal liver cells required for successful repopulation of abnormal erythrocyte precursor erythropoietic tissue by normal allogeneic precursors. This model system will establish the feasibility of selective erythrocyte repopulation as a method for correction of genetically determined erythrocyte diseases such as thalassemia. The test system will also be used to analyze the ability to restrict or eliminate graft rejection and graft vs host reactions involving fetal liver cells.